Further studies of the acute effects of phenylbutazone, oxyphenbutazone and indomethacin on the rat kidney

Arnold, L.; Collins, Catherine; Starmer, G. A.

doi:10.3109/00313027609094439

Cited by 19 publications

(4 citation statements)

References 8 publications

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“…The renal lesions described in this report are comparable to those reported as analgesic nephropathies in man [6,8,91 and rats [ 1,2,12,13,191. A characteristic renal lesion described in man [8,12,191 and rats [ 1, 2, 10, 121 is necrosis of the tips of the pyramidal medulla and is classified as renal papillary necrosis.…”

Section: Discussionsupporting

confidence: 76%

Renal Medullary Crest Necrosis Associated with Phenylbutazone Therapy in Horses

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1983

Vet Pathol

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Abstract. Thirty-five cases of renal medullary crest necrosis morphologically similar to the renal papillary necrosis of analgesic nephropathy as described in man and rats are reported in horses receiving maintenance dosages of phenylbutazone. The primary lesion is a well-demarcated focal medullary necrosis resulting in sequestration of fragments of the renal crest. Renal cortical lesions are considered secondary to the medullary necrosis and consist of segmental pallor as a result of tubular dilatation, filtrate retention, and interstitial edema. Ischemia in concert with phenylbutazone is suggested as the etiology. Renal medullary crest necrosis is presented as more appropriate morphological terminology for this lesion in the equine species than renal papillary necrosis as is used in man and rats.The nephrotoxicity of non-steroidal anti-inflammatory drugs in man is well known [8,12, 191. The drugs most commonly implicated in analgesic nephropathy are aspirin, phenacetin, and caffeine [ 121, although the phenylalkalonic acids fenoprofen, naproxen, and phenylbutazone also are incriminated [6, 1 1, 12, 181. A characteristic lesion of analgesic nephropathy is renal papillary necrosis [8,12, 191, and this lesion has been produced experimentally in rats with phenylbutazone and indomethacin [ I , 21 and in rats and rabbits with phenacetin and salicylates [ 3 , 101 and demonstrated to be the result of medullary ischemia [9, 131. Phenylbutazone is the most popular and widely used non-steroidal anti-inflammatory agent in equine medicine [4,7, 16, 171; however, morphological lesions associated with phenylbutazone toxicity in horses have been reported only rarely [5. 14, 151. Experimentally induced phenylbutazone toxicity in ponies has resulted in oral, gastric, duodenal, cecal, and colonic ulcers [ 14, 151. In an unrelated study in Thoroughbred and Standardbred horses, phenylbutazone produced oral and gastric ulcers in two horses [ 5 ] . Necrotizing phlebitis of the portal vein also was attributed to phenylbutazone toxicity [5].Although renal lesions commonly are ascribed to analgesic toxicities in man [8, 121 and rats [ l , 2, lo], no morphological lesions associated with the clinical use of phenylbutazone have been described in the kidneys of horses. The purpose of this paper is to report the spontaneous occurrence in 35 horses of renal medullary crest 662

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Section: Discussionsupporting

confidence: 76%

Renal Medullary Crest Necrosis Associated with Phenylbutazone Therapy in Horses

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1983

Vet Pathol

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“…The phytate levels found in tissues and blood in mammals clearly depend on dietary intake and these levels correlate with that found in the urine (12,27,33). Here, we show that phytate can be also readily absorbed from skin and might be clinically useful route of administration in subjects who are prone to the development of renal calculi.…”

Section: Discussionsupporting

confidence: 67%

“…Papillary calcification can be induced in rats with a combination of aspirin and sodium saccharin (30,31) and calcification of the vasa recta can be induced by long term phenacetin (32). Other studies demonstrated that high doses of phenylbutazone, oxyphenbutazone and indomethacin in rats leads to tubular necrosis in the lower nephron and causes calcification (33). Renal papillary necrosis and calcification also develop in diabetes mellitus (34).…”

Section: Discussionmentioning

confidence: 99%

Phytate acts as an inhibitor in formation of renal calculi

Gráses

Isern²,

Sanchís³

et al. 2007

Front Biosci

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The aim of this study was to assess the inhibitory action of phytate in formation of renal calculi. Hypertension (induced by nicotine) combined with hypercalcemia (induced by D vitamin) was used to induce calcification in renal tissue in male Wistar rats that were fed a purified phytate free diet. Phytate non-treated rats developed significant calcium deposits in kidneys and papillae, as well as in kidney tubules and vessels, whereas calcium deposits were absent in control and phytate treated rats. Fragments of hydroxyapatite (HAP) calculi exhibited the capacity to induce the growth of calcium salts on their surfaces. Presence of 1.5 mg/L of phytate in the synthetic urine inhibited the formation of calcium oxalate monohydrate on HAP renal calculi in normocalciuric conditions. The findings show that the action of phytate as a crystallization inhibitor takes place both in the intrapapillary tissue and urine.

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“…A number of studies demonstrating the potential of various nonsteroidal antiinflammatory drugs for causing papillary necrosis in animals (Arnold et al, 1976) have been reported and a few cases of papillary necrosis in individuals consuming these agents have appeared (Hussert et aI., 1979;Lourie et al, 1977). There is as yet, however, no proof of an important association between the use of nonsteroidal antiinflammatory drugs and the development of chronic renal disease.…”

Section: Introductionmentioning

confidence: 98%

Nephrotoxic Mechanisms of Drugs and Environmental Toxins

Porter¹

1982

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Further studies of the acute effects of phenylbutazone, oxyphenbutazone and indomethacin on the rat kidney

Cited by 19 publications

References 8 publications

Renal Medullary Crest Necrosis Associated with Phenylbutazone Therapy in Horses

Renal Medullary Crest Necrosis Associated with Phenylbutazone Therapy in Horses

Phytate acts as an inhibitor in formation of renal calculi

Nephrotoxic Mechanisms of Drugs and Environmental Toxins

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